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石英暴露与重度矽肺:肺门淋巴结的作用

Quartz exposures and severe silicosis: a role for the hilar nodes.

作者信息

Seaton A, Cherrie J W

机构信息

Department of Environmental and Occupational Medicine, University of Aberdeen Medical School, Scotland.

出版信息

Occup Environ Med. 1998 Jun;55(6):383-6. doi: 10.1136/oem.55.6.383.

Abstract

BACKGROUND

Two stonemasons working together in an environment with high concentrations of quartz pursued very different clinical courses; one died of rapidly progressive silicosis and the other developed hilar adenopathy and, later, early massive fibrosis. The exposures to quartz of these two men were investigated to allow comment on the pathogenesis of severe silicosis relative to concentrations of dust.

METHODS

Estimates of exposure were based on previously taken personal dust samples, detailed lifetime occupational histories, and semiquantitative exposure modelling.

RESULTS

One of the men who died had a 30 year exposure estimated to have averaged < 0.1 mg/m3, leading to hilar node fibrosis and calcification, followed by a five year exposure to about 2 mg/m3 which proved fatal. Estimates of exposure tallied with postmortem measurement of lung burden, suggesting retention of all dust deposited in the lungs over his final period of work. The younger man, working from the start of his apprenticeship alongside the older one, had a six year exposure to about 1.5 mg/m3, which caused hilar node enlargement and subsequent calcification but minimal lung involvement.

CONCLUSIONS

Exposures to relatively low concentrations of quartz may be capable of causing hilar node fibrosis, impairing the clearance of any quartz inhaled subsequently. The findings support the concept that destruction of the hilar nodes by silicotic fibrosis, impairing lung clearance, has an important pathogenic role in the development of massive fibrosis, and in men subsequently exposed to very high concentrations of respirable quartz, rapidly progressive silicosis.

摘要

背景

两名石匠在石英浓度高的环境中一起工作,但临床病程却大不相同;其中一人死于快速进展性矽肺,另一人出现肺门淋巴结病,随后发展为早期大块纤维化。对这两名男子的石英暴露情况进行了调查,以便就重度矽肺的发病机制与粉尘浓度的关系进行讨论。

方法

暴露估计基于之前采集的个人粉尘样本、详细的终生职业史以及半定量暴露模型。

结果

死亡的其中一名男子有30年的暴露史,估计平均暴露浓度<0.1毫克/立方米,导致肺门淋巴结纤维化和钙化,随后5年暴露于约2毫克/立方米的环境中,最终致死。暴露估计值与死后肺负荷测量结果相符,表明在其最后工作期间沉积在肺部的所有粉尘均被保留。较年轻的男子从学徒期开始就与年长的男子一起工作,有6年暴露于约1.5毫克/立方米的环境中,这导致肺门淋巴结肿大并随后钙化,但肺部受累最小。

结论

暴露于相对低浓度的石英可能会导致肺门淋巴结纤维化,损害随后吸入的任何石英的清除。这些发现支持了这样一种观点,即矽肺纤维化破坏肺门淋巴结,损害肺部清除功能,在大块纤维化的发展以及随后暴露于极高浓度可吸入石英的男性快速进展性矽肺的发生中具有重要的致病作用。

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